Preconceptual/prenatal care of our children: On the ethics of drug-induced disabilities

- Irina Pollard, Ph.D.

School of Biological Sciences, MacQuarie University, Sydney, NSW 2109, Australia


Eubios Journal of Asian and International Bioethics 6 (1996), 2-6.
Key Words: Nicotine, Alcohol, Ethanol, Caffeine, Intrauterine Growth Retardation (IUGR), Low birth-weight, Birth defects, Drug-consumption, Preconceptual period, Pregnancy, Xenobiotic, Teratogen, Bioethics.

Abstract

This article is concerned with the urgent need to view reproduction as a privilege and raises ethical issues concerning preventable congenital disorders resulting from maternal and paternal drug abuse. It concludes that morally it is inescapable that individuals have to take responsibility for their actions in respect of their unborn children. A caring society is also expected to preserve the fundamental human fetal right of protection and respect the right to a quality of life as dictated by the individual's genetic potential. Methods of influencing potential parents by involving the personal/collective continuum of responsibility, without infringement of individual rights, are discussed.


Introduction

Ignorance of lifestyle effects can be responsible for handicapping potentially healthy individuals. Common preventable drug-induced adverse outcomes of reproductive function include intrauterine growth retardation (IUGR), preterm birth, spontaneous abortion, early fetal death, increased risk of malformation and long-term defects of physical, mental and behavioural development (1,2). Reproduction under good conditions creates a positive force in shaping human identity. On the other hand, a stimulus or insult at a critically sensitive period in pregnancy may affect fetal growth and development, permanently weakening or impairing the subsequent normal function of the organ systems. If the induced changes involve the germ line cells, then such disturbances can be passed on by male, as well as female, parents and persist for multiple generations. Put simply, environmental effects are operative at all times during the differentiation of the gametes (sperm and eggs) so the health and living conditions of both parents from the time of gamete formation to the conception of the offspring is crucial, as is the maternal environment during pregnancy.

Low birthweight (2,500g or less) is a major cause of infant mortality, with most deaths occurring in the neonatal period. Inadequate fetal growth may result from prematurity (preterm delivery where the duration of pregnancy was less than 37 weeks from the last menstrual period), or poor fetal weight gain for a given duration of pregnancy (IUGR), or both. In general, the lowest risk of neonatal death and the greatest likelihood of optimal physical and intellectual development is in children weighing 3,000 g or more at birth (3,4). The neonatal mortality rate in affluent societies has dropped substantially since the late 1970s, but it has not been due to a decrease in the incidence of low-weight births. Instead, this mortality decline has been accomplished primarily by improving the chances of survival of low birth-weight infants through neonatal intensive care technology (5). About 7% of Australian babies are born low birth-weight (i.e. 2,500 g or less) with about 1% below 1,500 g and about 4% of all births involve some form of congenital abnormality visible at birth. The risk of major malformation is increased to 8-9% if one includes delayed developmental abnormalities, for example, mental retardation, behavioural anomalies and childhood cancers in the postneonatal period (6).

In affluent western countries there are racial determinants of infant mortality and morbidity. For example, the level of infant mortality (two to three times the national average) and low birth-weight (13%) is the highest among the Australian Aboriginal population (7,8). This exceptionally high reproductive morbidity is associated with poor living conditions and can be improved with heightened personal awareness and rising socioeconomic standards. For contemporary Aboriginal Australians many health outcomes are poor (9) because, relative to the general population, they have a lower family income, a lower education level (education is associated with increased spacing of children), have a greater percentage unemployed and frequently live in unacceptably overcrowded housing with poor sanitation. As a consequence, in the 35-44 year old age group (the reproductive years) medical problems related to alcohol consumption are the most frequently reported (10). In the United States of America, socio-environmental factors are similarly responsible for the significantly higher than average prevalence of birth defects among offspring born to Black women younger than 35 years of age (11).

This manuscript defends the case for provision of optimal conditions for reproduction and reviews the special biological and behavioural problems associated with intentional exposure to hazardous chemicals. The effects of smoking, alcohol and caffeine abuse in particular on reproduction are discussed. Because these three legal drugs are the most widely consumed, their impact is greater in terms of numbers of affected individuals, than the combined effects of illicit drug abuse. Approximately 29% of all patients referred for obstetric, pediatric or genetic treatment have a significant history of drug exposure (12). Although assisted reproductive technology (ART) currently is considered as a potential solution for most infertility problems regardless of the etiology, it should be remembered that this is associated with a wide range of complications that may endanger the offspring (13-17). All patients, even those where fertility has been compromised by excessive use of recreational drugs, with infertility problems are referred for treatment provided by the assisted reproductive technologies. In addition, ARTs are increasingly being used for male-mediated infertility (18). Prenatal parental abuse (a form of child abuse) resulting in a compromised offspring is not consistent with respect for human life. The view that it is a moral crime (both against the unfortunate offspring and against society) to bring a child into existence without fair prospects, is not yet widely publicised. This review is an attempt to integrate prenatal care into a holistic view of reproductive behaviour. The scientific basis for the findings and ethical issues generated here are more fully developed in my recent textbook (1).


The Clinical and Epidemiological Data

This paper excludes discussion of the results of animal experimentation and concentrates on the human data from recently published clinical and epidemiological articles.


1.1 Nicotine: Maternal Cigarette Smoking

It has to be emphasised that cigarette smoking has emerged as the single most important preventable cause of poor health, disease and death in the industrialized world (19,20). Fortunately, people are increasingly aware of the dangers to the adult of tobacco use but the impacts of ill-health on reproduction is not as well publicized or recognised. Smoking among young women aged between 18 and 24 years has steadily increased with approximately 30% of women in their reproductive years smoking (21). Smoking among girls younger than 16 years is also rapidly increasing. It has been estimated that smoking is responsible for 20-35% of all low birth-weights and a decrease in perinatal mortality of 10% could be expected if all women stopped smoking during pregnancy (22). Maternal tobacco use has been strongly implicated in many adverse outcomes of reproductive function; including increased infertility (23), ectopic pregnancies (24), infant low birthweight due to IUGR and prematurity (25), miscarriage and early fetal death (26), increased risk of certain birth defects (27) and long-term defects of growth and behavioural development (28). The extent of the above outcomes is directly proportional to the number of cigarettes smoked. There is also a relationship between smoking during pregnancy and Sudden Infant Death Syndrome (SIDS) (29), with the risk increasing with increasing number of cigarette smokers surrounding the already IUGR infant (30). Exposure to tobacco during pregnancy can also affect the reproductive capacity of the next generation as fecundity is decreased in daughters (31) and sperm defects are more frequent in sons (32) of smoking mothers. Even though the children become in turn non-smoking parents, they may perpetuate the adverse effects caused by their parents' smoking habits - a classical case of grandparents modulating the reproductive health of their grandchildren.

Specific abnormalities noted in the offspring born to smoking mothers were cardiovascular, urogenital, microcephalus, neural tube defect, lip and palate cleft and club foot (26). However, the association between smoking during pregnancy and the increased risk of any one specific congenital abnormality in the offspring depends on the presence of other risk factors, population heterogeneity and innate genetic strengths or weakenesses in the nicotine-exposed fetus, as stresses are cumulative. Smoking is also associated with an increased risk of spontaneous abortion so the magnitude of the relationship between maternal smoking and congenital malformations at birth is correspondingly reduced. Birth registers which provide the data for the population-based studies underestimate the true numbers of birth defects as they only record malformations present at birth. Studies of negative effects of smoking on various aspects of mental development, such as reading performance, have been made. Children tested at the ages of 7 and 11 had, on an average, a three month delay in general development if their mothers had smoked over 10 cigarettes per day during the pregnancy. They also had a four months delay in reading performance and a five months delay in mathematical skills (33). A correlation between the number of cigarettes smoked during pregnancy and cancer risk in the child is statistically established; smoking doubles the risk of non Hodgkin lymphoma, acute lymphoblastic leukemia and Wilm's tumour (34). Smoking significantly influences lactation. Vio and Salazar (35) found that reduced milk production in smoking mothers correlated strongly with decreased weight increments in the suckled babies. Another study reported a significant reduction in both the mean milk volume and milk fat concentration among mothers who smoked and gave birth to a low birth weight infant (36). For these unfortunate babies the nicotine-contaminated breast milk continues the stunting effect already commenced in utero.

The effects of passive smoking are also well documented (37); children whose parents smoke suffer more lower (cough, wheeze, bronchitis, pneumonia), and upper (colds, influenza, pharyngitis, tonsillitis) respiratory tract diseases than children whose parents do not smoke. Pregnant women exposed to others' cigarette smoke may also be more likely to deliver a low-birthweight infant (38). The common diseases of passive smoking can be life-threatening because repeated lower respiratory tract illness in the young may give rise to impaired lung function and the development of more serious chest disease such as asthma, later in childhood and in adulthood.


1.2 Nicotine: Paternal Cigarette Smoking

The majority of common risk factors apply to both sexes but much less publicity is given to paternally-mediated drug effects on the offspring. Male reproductive function may be altered by chronic exposure to bioactive compounds like nicotine, ethanol and caffeine because the drugs move from the blood to the testes where they interrupt hormone synthesis and secretion and influence differentiation of the germinal cells. Because sperm cells are particularly vulnerable to damage, genetic abnormalities are more often linked with paternal than with maternal DNA damage (39) and morphological abnormalities in the sperm are prevalent among individuals who smoke (40,41). Smoke condensates are mutagenic (37), providing a logical mechanism by which male smokers may transmit teraspermic effects to their offspring. While the frequency of abnormal sperm increases, other semen parameters, such as sperm density (number), motility and fertilizability, are significantly decreased in smokers (42,43). As a consequence of poor sperm quality, children of non-smoking mothers whose fathers smoke have a greater chance of being born low birth-weight and suffer an increased incidence of perinatal mortality (44). These early findings have since been corroborated and extended. Paternal smoking is associated with a clinically significant, dose-dependent retardation in fetal growth (45). Independently of parental age and social class, the frequency of severe malformations is doubled in children of non-smoking mothers when the father smokes more than 10 cigarettes per day (46). Birth defects increased by passive smoking include hare-lip, heart defects and abnormal narrowing of the urethra. Childhood cancers are also significantly more common among children whose fathers smoked at the time of conception; leukaemia and cancer of the lymph nodes being twice as common and brain cancer 40% more common among the children of men who had smoked in the year before their children were born (47).

In males, smoking leads to increased estrogen and decreased testosterone serum levels (48). This effect is mostly mediated via changes in adrenal function due to the release of stress hormones such as adrenaline and cortisol. Low testosterone causes, in turn, low sperm count and motility. Much of the damage is caused by oxidising compounds in cigarette smoke and when oxidation outstrips the body's repair mechanisms the DNA is irreversibly damaged (49). It is unfortunate for the next generation that common non-adaptive lifestyles such as smoking are often duplicated, with both mother and father contributing genetic and epigenetic burdens on the development of their fetus.


1.3 The Benefits of Quitting Smoking

Almost all the literature on the reproductive benefits of quitting is concerned with the habit in females so I cannot gender balance this section. About 30% of all women quit on their own initiative when they realize that they are pregnant (49) and the quitting rate is higher in women with longer education. Verification of a pregnancy induces a phase of pre-contemplation leaving the mother-to-be open to many influences (50). This provides an opportunity that should not be missed; health education is both efficacious and cost beneficial. Reduction in the consumption of cigarettes, negative attitudes towards smoking and determination to stop smoking is significantly higher among women who are encouraged by their partners to stop smoking and in those who perceived that their partners were willing to reduce their consumption. Single women smoke more often than women living with a partner. However it is clear that quitting is a complex undertaking which requires will-power and specific knowledge since despite serious and well-established risks to the offspring a significant number of women continue to smoke throughout pregnancy (51). The need for a national campaign to disseminate smoking cessation methods to those who are contemplating reproduction is obvious. The good news for women who quit before conception is that their fertility is no different from that of non-smokers and ex-smokers' pregnancies seem to be as successful as those of non-smokers.


2.1 Ethanol: Maternal Drinking

Alcohol causes central nervous dysfunction (52) by changing neurotransmitter release and neuronal function in the brain's most integrative areas. It exerts its most profound central nervous system (CNS) effects during the fetal period. Of women 18-29 years of age, an estimated 21% are moderate drinkers (4-13 drinks/week) or heavy drinkers (2 or more drinks/day). Alcohol use by pregnant women is highest in smokers (37%) and the unmarried (28%) (2). Alcohol-induced effects, in addition to those on the CNS, are not unlike those described for nicotine; i.e., prenatal loss, fetal growth retardation and developmental defects. Alcohol-related teratogenic effects are usually clustered and can be clinically recognized as the Fetal Alcohol Syndrome (FAS). The average IQ of the FAS children is about 70; and the severity of mental retardation and behavioural problems is related to the degree of alcohol exposure in utero (53). Of all the characteristics of FAS, mental retardation is the most damaging and consistent consequence and is now the leading cause of mental retardation in the western world (54). It has been estimated that the incidence, worldwide, of FAS is 2 cases per 1,000 live births and, for the population most at risk, rises sharply to as high as 59 per 1,000 live births (55). Since pre- and/or postnatal growth retardation is one of the diagnostic features of FAS, there is also a significant additional number of children who suffer from debilitating lifetime alcohol-related defects.

Prenatal/preconceptual exposure to ethanol has been linked to immune deficits, increased frequencies of malignancies (56) and behavioural anomalies including short attention span, easy distractibility and hyperactivity (57), in the offspring. About 70% of FAS children suffer from attention deficit disorders even when their IQ scores are normal (57). As a consequence, FAS victims have emotional problems which may later translate to poor cognitive performance in school.

The detrimental consequences of alcohol consumption during pregnancy have been known since antiquity. Aristotle warned that women drunkards often gave birth to abnormal children and the consumption of alcoholic beverages by young married couples was prohibited in ancient Greek and Old Testament writings (58). Apart from the personal tragedies, the costs of providing treatment to children with FAS have conservatively been estimated for the USA at about US $230 million annually and mental retardation accounts for almost 60% of this (59). Despite this enormous outlay many children with special needs are still neglected because the requirements outstrip the available resources (treatment costs are particularly high for those with IQ scores from 50 to 65).

Research on the possible teratogenic mechanisms involved in FAS has focussed on direct alcohol toxicity, acetaldehyde (metabolite) toxicity, fetal hypoxia, nutritional deficits and placental dysfunction (1). Other factors which frequently accompany alcoholism may also contribute to FAS. These include maternal and paternal smoking, caffeine and other drug consumption. The relationship between maternal alcohol consumption and the risk of FAS is difficult to quantitate as there are critical periods during pregnancy when the fetus is exceptionally susceptible. Isolated facial anomalies are more likely to result when alcohol ingestion is confined to early pregnancy, whereas chronic alcohol consumption throughout pregnancy results in growth retardation and a wide variety of structural/functional defects (60). Existing dogma holds that consumption of large amounts of alcohol at one time (binge drinking) is more detrimental than one or two drinks daily, which is generally but not universally accepted as being safe (61). A number of other variables including nutritional status, whether the woman was a heavy drinker preceding her pregnancy, multiple drug use (polydrug abuse usually includes cigarette and marijuana use and, increasingly, cocaine abuse), stressful life situations and genetic factors all interact with alcohol in the development of FAS. It can be argued that since no safe level of alcohol intake has been established, women would be wise to abstain completely from drinking during pregnancy and whilst attempting to conceive.

Postnatal growth and neuroanatomical development is also adversely affected by exposure to alcohol-contaminated breast milk. Growth deficiency continues over the period of breast-feeding due to a combination of nutritional deficits and toxic drug effects.


2.2 Ethanol: Paternal Drinking

An effect of paternal drinking on the fetus has been suggested by epidemiological analyses (62-64). The relationship, as for nicotine, depends on alcohol-induced changes in sperm and relates to the mutagenic properties of the drug. Alcoholism has long been known to cause testicular atrophy, desquamation of the germinal epithelium, decreased sperm motility, oligo- and teraspermia, decreased testosterone production, loss of libido and impotency (brewer's droop!) (65). Alcoholic males can influence the health prospects of their children genetically through decreased quality of gametes.


3.1 Caffeine: Maternal Consumption

Caffeine, a trimethylxanthine alkaloid, is the most widely consumed psychophysiologically active substance in the world. It is readily available in coffee (containing from 85 to 110 mg/cup), tea (about 50 mg/cup), cola beverages (30-45 mg/serving), cocoa (about 5 mg/cup), chocolate (25 mg/small bar), as well as preservatives, analgesics and other pharmaceutical preparations. The average daily adult caffeine intake of moderate to heavy consumers is about 463 mg/day or the equivalent of 5-6 cups of brewed coffee. The drug's popularity is also reflected in the number of children consuming caffeine-containing substances.

Caffeine is a powerful CNS stimulant, with theophylline (a major active component in tea) and theobromine (a major active component in cocoa beans) having less potent effects. Caffeine has a number of other general stress-like effects, such as catecholamine release, mobilization of free fatty acids, increased metabolic and heart rates and altered blood pressure. Structurally, methyl-xanthines are purine alkaloid analogues of the purines found in the nucleic acids RNA and DNA. Because the methylxanthines are purine analogues, they interact chemically with DNA in different ways and may intercalate and/or disorganize its helical structure. This characteristic may result in the retention of faulty chromosomal rearrangements in sperm, maturing oocytes and rapidly dividing embryos (66). Caffeine is a strong potentiator of adverse reproductive effects when co-administered with other drugs exacerbating the toxic effects of nicotine and ethanol. For this reason epidemiological studies of caffeine effects are sometimes contradictory. In general, pregnant women reduce their caffeine intake; however, 70-85% still continue to consume some caffeine throughout their pregnancies, with an estimated 18% consuming amounts equivalent to four or more cups of coffee daily (67).

Moderate caffeine intake is a risk factor in infertility, fetal loss and fetal growth impairment (68). While the subfecundity (typically defined as prolonged time to conception) studies are equivocal, there is reasonable evidence for a dose-dependent caffeine effect on fertility. Women who drank more than one cup of coffee daily were half as likely to conceive as those who drank less than one cup a day (69), and women who consumed more than 7,000 mg caffeine monthly (about 21/2 cups daily) were 4.7 times less likely to conceive than women who consumed less than 5 cups of coffee per month (68). Caffeine-induced subfecundity may well be the result of unrecognized spontaneous loss of defective pregnancies, rather than a failure to conceive.

Caffeine has a variety of teratogenic effects even at a moderate level of intake. Women drinking more than 3 cups of coffee per day during the first trimester have an increased risk of miscarriage (70) and caffeine consumption prior to and during pregnancy is associated with prematurity, fetal IUGR and neonatal withdrawal symptoms (66). Since caffeine has not been studied as extensively as nicotine or ethanol, the drug's effects on human development are not fully known. As little as 150 mg caffeine (equivalent to 2-3 cups of coffee) per day during pregnancy can result in lowered infant birth-weight and its use accounts for up to 6% of all cases of IUGR (71). Infants exposed to high levels of caffeine in utero may suffer withdrawal symptoms (irritability, jitteriness and vomiting) after delivery (72). This withdrawal dysfunction may also be a potentiating factor in neonatal apnoea and SIDS (73).


3.2 Caffeine: Paternal Consumption

A relationship between paternal caffeine exposure and adverse pregnancy outcome has been reported (74). This association is not surprising because caffeine in blood rapidly enters the semen. Stresses are cumulative and a synergistic effect of caffeine consumption, cigarette smoking and alcohol intake on semen quality has been demonstrated (75). The combination of smoking and drinking more than four cups of coffee a day significantly decreases sperm motility, reduces sperm density and increases the percentage of dead sperm (75). 


Discussion

Ethical Consideration: Conflict Between Parental, Societal and Child's Interests

Fetal rights (unqualified by quality of life issues) have been among the most prominent and bitterly contentious of reproductive options. In the 1990s, life-sustaining support for infants having drug-induced prematurity and growth retardation results in smaller and smaller neonates spending longer and longer periods developing in incubators. No-one knows what the long-term effects of such artificial beginnings will be on the offspring and offspring-bonding capabilities. The paramount issue of what is in the "best interest" of the child is sometimes lost in the public discussion of the "indisputable" right of the parents to determine these interests on their child's behalf. There is an urgent need for open debate about the morality of drug abuse when a child's genetic potential is the issue. Can fetal rights issues be unqualified by quality of life issues? Passive acceptance of the negligent violation of this basic fetal right can only strengthen the cynical view that the birth of a child has political rather than biological value.

Aside from the ethical considerations in respect of the growth retarded fetus, the costs to society of the current technological intervention must also be evaluated. The following table compares the costs of looking after Australian neonates of differing degrees of disability.

Comparative costs of treatment by hospital admission*
Extreme immaturity in neonate $24,623
Prematurity with major problems $18, 506
Term neonate with major problems $3, 945
Normal newborn $1,424

*Source: Manual of Resource Items and Their Associated Costs. Department of Health, Housing and Community Services, 1992.

Neonatal intensive care of low birthweight infants born in Victoria, Australia, during 1985-87 cost the community A$104,990 for each survivor or A$5,390 for each additional year of life gained (76). Similarly, figures compiled by the Centres for Disease Control show that in the United States of America more than 10% of babies are born prematurely and, according to a 1985 U.S. National Academy of Sciences report, some $5 billion is spent on these infants, mostly for high-tech neonatal care (77). Much of the debate over neonatal intensive care units (ICUs) is based on the distribution of scarce resources among many demands and if some baby's lives are being saved it is only because the decision has been made to spend generously. Others, rural Aboriginal babies for example, do not have access to ICUs nor adequate housing, water or immunisation programs. These babies, whose living conditions increase the incidence of low birth weight are dying because the commitment is not enough. In this, as in so many health areas, the community tolerates the overriding of ethics by economics.


Ethical Consideration: Preventitive Strategies, Social Action and Cultural Change

In the past, too much reliance has been placed on the power of technology and hospital treatment to correct post-partum problems but healthy pregnancies begin well before conception. Education about reproduction, contraception, pregnancy and the responsibilities of being a parent will alleviate some of the worst cases and eliminate a good proportion of marginal cases of preventable growth retardation. Not many parents knowingly want to handicap their offspring. Additional effort spent in preconception/prenatal education is socially desirable, as unmet needs are greatest among the poor and the young; two groups at high risk of having low birthweight infants. Infants weighing 2,500 g or less at birth impose a large economic burden on the whole community, initially through the need to provide neonatal care, and, subsequently in health and disability care of surviving infants and adults. The provision of adequate educational assistance and prenatal care can be covered from cost savings in the care of low birthweight children. Savings through prevention of low birthweight should, in the long-term, more than offset the additional cost of prevention programs.

We ought not to underrate the potential influence of the individual because it is generally accepted that societal change is dependent on the collective. If we are going to embrace fundamental social change and protect future children without threatening parents' fundamental freedoms, then new beliefs and priorities must evolve from the general public and, eventually, become the status quo. In the final analysis, the collective is dependent on being able to persuade a critical mass of individuals to move in the same direction and when a consensus or agreement that some things are more important than individual parochial self-interest is reached, change is imminent. The established bioethical principles of autonomy, beneficence and/or nonmaleficence and justice must be utilized to highlight the citizen's moral obligations consequent on new research-driven understanding of behavioural effects on reproduction. The development of an effective health program that assures preventitive care for all, is consistent with a commitment to beneficence and social justice. Since research has provided a scientific basis of assessing reproductive outcomes, debate about the human person and the good society must also clearly state its strong opposition to the needless handicap of the fetus. Each person has a right to bodily integrity involving both preventitive and curative health care; a right endorsed by the responsible individual person and by society. A future society may choose not to tolerate parental deficiencies in adaptive behaviour which compromise the dignity of future generations and, indeed, possibly the most challenging decision anyone may ever face could well be whether or not to become a parent. Translating preventitive care into action requires an educational framework which creates a favourable culture accepting of the moral obligation that all of us are, to a considerable degree, custodians of the next and subsequent generations. Such a moral framework may even be supported by public policy demonstrating a solidarity with individual values enshrined in the acceptance of reproduction as a privilege rather than a right; a right which is all too often taken lightly.

A new, socially acceptable code of reproductive conduct may be followed by incorporation into legislative policy. A bill of rights guaranteeing all a minimum standard of education in the range of social, economic and environmental issues relevant to the present discussion would, in turn, reinforce the accepted culture by democratic processes. Appropriate legislation would lay down educational foundations for ensuring that children are educated so that they can, in the future participate fully in fair and just parenting. Debate presaging such a bill would encourage full participation by individuals and public bodies (teachers' unions, for example). The democratic process would have total societal protection since the participation, accelerated by social processes, originated from an heightened sense of public justice.

As to the question of who would educate the answer would be the personal/collective continuum. Public understanding enhanced by scientific findings will form the backdrop to sympathetic communications between experts and the population. Education that not only covers disease, but prevention, needs grass-roots projects. The social process might begin by making efficient use of retired, elderly and unemployed people previously involved in health-care, teaching and politics etc. Among this mostly underutilized pool of professionals are brilliant, creative and experienced individuals looking for stimulation, challenge and the opportunity to give something back to their society. Such a cost-effective scheme has many beneficial aspects not only for future children but even for the volunteers. There is research demonstrating that useful volunteering releases endorphins that heighten the joy of living and strengthen the immune system (78). The commercial sector should also be involved. For example, manufacturers of contraceptive products and formulations could be persuaded to provide free preconceptual care information in their packaging. Such a service seems logical and socially desirable since contraceptive suppliers are already in the business of improving reproductive outcome by preventing unwanted births. Other beneficial aspects involve cost transfer from the care of low birth-weight children to providing adequate educational assistance, prenatal care and other prevention programs.

In conclusion I wish to pose the following three questions, acknowledging that they are confronting and are certain to attract controversy.

Accepting that the unborn has a basic human fetal right to bodily integrity, should there be constraints on what can be ethically done to the unborn? Can a community be caring if it fails to preserve the fundamental human right of protection from serious prenatal abuse? Can the indisputable right to be a parent be upheld if the expression of the offspring's genetic potential is knowingly denied?


Acknowledgements

I thank Dr R.G. Hiller for helpfully commenting on the manuscript. 


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